In a recent study, a group of psychologists decided to see if this differential reaction is simply behavioral, or if it actually goes deeper, to the level of brain performance. The researchers measured response-locked event-related potentials (ERPs)—electric neural signals that result from either an internal or external event—in the brains of college students as they took part in a simple flanker task. The students were shown a string of five letters and asked to quickly identify the middle letter. The letters could be congruent—for instance, MMMMM—or they might be incongruent —for example, MMNMM.

While performance accuracy was generally high, around 91 percent, the specific task parameters were hard enough that everyone made some mistakes. But where individuals differed was in how both they—and, crucially, their brains— responded to the mistakes. Those who had an incremental mindset (i.e., believed that intelligence was fluid) performed better following error trials than those who had an entity mindset (i.e., believed intelligence was fixed). Moreover, as that incremental mindset increased, positivity ERPs on error trials as opposed to correct trials increased as well. And the larger the error positivity amplitude on error trials, the more accurate the post-error performance.

So what exactly does that mean? From the data, it seems that a growth mindset, whereby you believe that intelligence can improve, lends itself to a more adaptive response to mistakes—not just behaviorally but neurally. The more someone believes in improvement, the larger the amplitude of a brain signal that reflects a conscious allocation of attention to errors. And the larger that neural signal, the better the subsequent performance. That mediation suggests that individuals with an incremental theory of intelligence may actually have better self-monitoring and control systems on a very basic neural level: their brains are better at monitoring their own, self-generated errors and at adjusting their behavior accordingly. It’s a story of improved online error awareness —of noticing mistakes as they happen, and correcting for them immediately.

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Women who are given examples of females successful in scientific and technical fields don’t experience the negative performance effects on math tests. College students exposed to Dweck’s theories of intelligence— specifically, the incremental theory—have higher grades and identify more with the academic process at the end of the semester. In one study, minority students who wrote about the personal significance of a self-defining value (such as family relationships or musical interests) three to five times during the school year had a GPA that was 0.24 grade points higher over the course of two years than those who wrote about neutral topics—and lowachieving African Americans showed improvements of 0.41 points on average. Moreover, the rate of remediation dropped from 18 percent to 5 percent.

Experience rearranges anatomical connectivity in the brain, but such plasticity is suppressed in adulthood. We examined the turnover of dendritic spines and axonal varicosities in the somatosensory cortex of mice lacking Nogo Receptor 1 (NgR1). Through adolescence, the anatomy and plasticity of ngr1 null mice are indistinguishable from control, but suppression of turnover after age 26 days fails to occur in ngr1−/− mice. Adolescent anatomical plasticity can be restored to 1-year-old mice by conditional deletion of ngr1. Suppression of anatomical dynamics by NgR1 is cell autonomous and is phenocopied by deletion of Nogo-A ligand. Whisker removal deprives the somatosensory cortex of experience-dependent input and reduces dendritic spine turnover in adult ngr1−/− mice to control levels, while an acutely enriched environment increases dendritic spine dynamics in control mice to the level of ngr1−/− mice in a standard environment. Thus, NgR1 determines the low set point for synaptic turnover in adult cerebral cortex.

Formation of lasting memories is believed to rely on structural alterations at the synaptic level. We had found that increased neuronal activity down-regulates Nogo receptor-1 (NgR1) in brain regions linked to memory formation and storage, and postulated this to be required for formation of lasting memories. We now show that mice with inducible overexpression of NgR1 in forebrain neurons have normal long-term potentiation and normal 24-h memory, but severely impaired month-long memory in both passive avoidance and swim maze tests. Blocking transgene expression normalizes these memory impairments. Nogo, Lingo-1, Troy, endogenous NgR1, and BDNF mRNA expression levels were not altered by transgene expression, suggesting that the impaired ability to form lasting memories is directly coupled to inability to down-regulate NgR1. Regulation of NgR1 may therefore serve as a key regulator of memory consolidation. Understanding the molecular underpinnings of synaptic rearrangements that carry lasting memories may facilitate development of treatments for memory dysfunction.

Experience may blind us from recognizing obvious solutions to problems. Research shows that physicians and health care professionals are likely to overlook the correct diagnosis in cases which do not match their experience [1]. Similar findings have been reported concerning difficulties in reframing clinical situations as experienced by healthcare professionals [2], [3], and difficulties of managers and decision makers in replacing existing procedures with new, improved and simpler ones [4]. This “blinding” to novel solutions may be considered a form of cognitive rigidity, which has commonly been defined as a resistance to change in beliefs, attitudes or personal habits [5], or the tendency to develop and perseverate in the use of mental or behavioral sets [6].

Such cognitive rigidity may play a key role in psychopathlogy (for reviews see [6], [7], see also [8]). It has been closely linked to the inability of suicidal individuals to consider alternatives that may be accessible to another person [9], [10], as well as to rumination, a major risk factor of depression [11]. Similar forms of cognitive rigidity were also indicated in obsessions [12], [13], alcohol dependence [14], eating disorders [15], and Attention Deficit Disorder [16]–[20]. In this paper, we propose that mindfulness meditation may provide a means of decreasing the aforementioned type of cognitive rigidity.

Plasticity is a double-edged sword; the more flexible an organism is the greater the variety of maladaptive, as well as adaptive, behaviors it can develop; the more teachable it is the more fully it can profit from the experiences of its ancestors and associates and the more it risks being exploited by its ancestors and associates.

My mind seems to have become a kind of machine for grinding general laws out of large collections of facts, but why this should have caused the atrophy of that part of the brain that alone on which the higher tastes depend, I cannot conceive. A man with a mind more highly organised or better constituted than mine would not, I suppose, have thus suffered, and if I had to live my life over again, I would have made a rule to read some poetry and listen to some music at least once every week; for perhaps the parts of my brain now atrophied would thus have been kept alive through use.

Past experiments have shown persuasively that exercise spurs the birth of new mitochondria in muscle cells and improves the vigor of the existing organelles. This upsurge in mitochondria, in turn, has been linked not only to improvements in exercise endurance but to increased longevity in animals and reduced risk for obesity, diabetes and heart disease in people. It is a very potent cellular reaction.

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Like muscles, many parts of the brain get a robust physiological workout during exercise. “The brain has to work hard to keep the muscles moving” and all of the bodily systems in sync, says J. Mark Davis, a professor of exercise science at the Arnold School of Public Health at the University of South Carolina and senior author of the new mouse study, which was published last month in The Journal of Applied Physiology. Scans have shown that metabolic activity in many parts of the brain surges during workouts, but it was unknown whether those active brain cells were actually adapting and changing.

To see, the South Carolina scientists exercised their mice for eight weeks. The sedentary control animals were housed in the same laboratory as the runners to ensure that, except for the treadmill sessions, the two groups shared the same environment and routine.

At the end of the two months, the researchers had both groups complete a run to exhaustion on the treadmill. Not surprisingly, the running mice displayed much greater endurance than the loungers. They lasted on the treadmills for an average of 126 minutes, versus 74 minutes for the unexercised animals.

More interesting, though, was what was happening inside their brain cells. When the scientists examined tissue samples from different portions of the exercised animals’ brains, they found markers of upwelling mitochondrial development in all of the tissues. Some parts of their brains showed more activity than others, but in each of the samples, the brain cells held newborn mitochondria.

There was no comparable activity in brain cells from the sedentary mice.

This is the first report to show that, in mice at least, two months of exercise training “is sufficient stimulus to increase mitochondrial biogenesis,” Dr. Davis and his co-authors write in the study.

Other, less tragic kinds of evidence also support this idea. Most people have a much more difficult time learning a second language late in life than they do in childhood. Immigrants may try to learn the language of their new country, only to be outdone by their own children. When we visit a foreign country for a while, our kids seem to be happily chatting with the other kids in the playground, while we are still painfully looking through the phrase books. When we learn a second language past puberty, we speak with a foreign accent—in other words, with phonetics, intonation, and stress patterns that are not appropriate for the new language. We also have more difficult)^ understanding spoken speech and more difficulty with the grammar of the language. Puberty seems to be an important time. An immigrant who speaks nothing but English from the age of eighteen on may still have a heavy accent in his old age; another immigrant who arrives at four years of age may have no trace of one.

Let me suggest a new axiom: juxtaposition is the spice of life. Humanity’s biggest talent, unique to us, is juxtaposing, finding and operating novel relationships between things or ideas... Recent ideas on neural activity suggest that the brain operates in a very associative way, with small neuron clusters containing core concepts, rather in the way a battery holds a trickle charge. These core concepts would be irreducibly small fragments of sounds or sights, or any phenomena that you experience. And these clusters are all, in some way, apparently interconnected, set up in microcolumns and macrocolumns, each column made up ofmillions of these lit,tle clusters of neurons. Now, if you consider that the brain passes information by means of synaptic junctions (the bits where one neuron almost touches another) and that there are potentially more of those kinds of connections in the brain than there are atoms in the known universe, you get a feel for the immensity of the network. With this associative system, to retrieve data, you go in, so to speak, anywhere on the network and find the target by association. Given the scale of things, an associative approach might be the only way the whole huge complex could work. Anyway, retrieval by association would be a good survival mechanism, because it would make you very flexible.